Downregulation of microRNA-9 increases matrix metalloproteinase-13 expression levels and facilitates osteoarthritis onset.

Matrix metalloproteinase-13 (MMP-13) degrades collagen and other matrix components, thus playing a critical role in the development of osteoarthritis (OA). The expression level of microRNA‑9 (miR‑9) is significantly depressed in cartilage tissues of OA patients. Furthermore, bioinformatics analysis demonstrated complementary binding sites between miR‑9 and MMP‑13. The current study, therefore, investigated whether miR‑9 is involved in regulating MMP‑13 expression levels and OA onset. Cartilage tissues from OA patients and healthy individuals were compared for miR‑9, MMP‑13 and collagen type II α1 chain (Col2A1) expression levels. A dual luciferase gene reporter assay was performed to evaluate the association between miR‑9 and MMP‑13. Sodium iodoacetate was injected into the knee joint cartilage tissues to generate the rat OA model. The expression levels of miR‑9, MMP‑13 and Col2A1 were compared between the model and control rats. In addition, the OA model rats received miR‑9 agomir for further expressional assay. Cartilage tissue samples from the OA patients exhibited significantly lower miR‑9 and Col2A1 expression levels when compared with the control rats, whilst the expression level of MMP‑13 was upregulated. As the target gene of miR‑9, MMP‑13 is under the targeted regulation of miR‑9. The injection of miR‑9 agomir into the knee joint cavity significantly depressed MMP‑13 expression in the cartilage tissues of OA rats, with reduced collagen degradation and enhanced COL2A1. OA cartilage tissues have lower miR‑9 expression and higher MMP‑13 expression levels. Thus, miR‑9 inhibits the expression level of MMP‑13, decreases its inhibitory effects on COL2A1, and therefore contributes to antagonizing OA.